scholarly journals Evaluation of colistin nephrotoxicity and urinary level of kidney injury molecule-1 in hospitalized adult ICU patients

2020 ◽  
Vol 9 (2) ◽  
pp. e13-e13
Author(s):  
Afsaneh Vazin ◽  
Maryam Malek ◽  
Iman Karimzadeh

Introduction: Colistin is a cationic polypeptide antibiotic used for treatment of gram-negative infections. Nephrotoxicity is one of the most common adverse effects of colistin. Objectives: To determine the epidemiology of colistin nephrotoxicity and also to compare the changing pattern of kidney injury molecule 1 (KIM-1) in urine with serum creatinine and urine during the treatment with colistin in patients admitted to intensive care unit (ICU). Patients and Methods: During 13 months, all patients admitted to adult ICUs of two university hospitals without any documented history of acute or chronic kidney diseases receiving at least one week of colistin were included. Required demographic, clinical, and paraclinical data of the study population was collected. Urinary and serum levels of creatinine, urea, sodium, potassium, magnesium, and KIM-1 were measured at six time points including days zero, 3, 5, 7, 10, and 14 of colistin treatment. Results: Six patients (18.18%) developed nephrotoxicity during colistin treatment. Nephrotoxicity was resolved without any intervention in three individuals. None of studied demographic, clinical and laboratory characteristics of the patients had a significant association with the incidence of colistin nephrotoxicity. The pattern of KIM-1 urine level during the course of colistin treatment did not differ significantly among patients with and without nephrotoxicity. The accuracy of KIM-1 urine level in detecting colistin nephrotoxicity was significantly lower than that of serum creatinine on days 0th, 3rd, 5th and 7th. Conclusion: Nephrotoxicity of colistin is a common complication, usually reversible, KIM-1 was not more accurate than serum creatinine or urine in detecting nephrotoxicity of colistin.

2021 ◽  
Author(s):  
Yuanyuan Pei ◽  
Guangping Zhou ◽  
Pengfei Wang ◽  
Fang'e Shi ◽  
Xiaolu Ma ◽  
...  

Abstract Background: Acute kidney injury (AKI) was a common and critical complication of sepsis, and is associated with unacceptable morbidity and mortality. Current diagnostic criteria for AKI was insensitive for early detection. Novel biomarkers included cystatin C, KIM-1, NGAL, klotho and FGF-23 which can predict AKI earlier may allow immediate interventions. We aimed to determine the diagnostic performance of these biomarkers for detecting AKI in sepsis patients.Methods: This prospective observational study was conducted from May 2018 and November 2020, enrolling sequential 162 sepsis patients. AKI’s definition was according to 2012 KDIGO criteria and we divided patients into non-AKI (n=102) and AKI (n=60) groups. Serum levels of several AKI biomarkers were detected by ELISA. The relationship between biomarker levels on admission of AKI were analyzed and discrimination performances comparison were performed.Results: AKI incidence was up to 37.0% (60/162) during hospitalization. Compared with non-AKI group, both serum cystatin C, KIM-1, NGAL and FGF-23 were significantly elevated at admission in septic AKI patients. The areas under the receiver operating curves demonstrated that serum cystatin C had modest discriminative powers for predicting AKI after sepsis, and cystatin C combined with serum creatinine in the prediction of septic AKI increased the diagnostic sensitivity prominently.Conclusion: Serum cystatin C, KIM-1, NGAL and FGF-23 levels are both increased in septic AKI patients. Our study provides reliable evidence that cystatin C solely and combined with serum creatinine may accurately and sensitively predict septic AKI when patients on admission.


2018 ◽  
Vol 69 (2) ◽  
pp. 375-378
Author(s):  
Catalin Pricop ◽  
Ileana Adela Vacaroiu ◽  
Daniela Radulescu ◽  
Daniel Andone ◽  
Dragos Puia

In the literature, occurrence of acute kidney injury (AKI) in young patients with unilateral ureteral lithiasic obstruction and without previous renal impairment is not very often reported, and the underlined pathophysiological mechanisms are poorly known; according to some studies, it is a false kidney failure, the increase in serum creatinine being due to absorbtion of obstructed urine in the affected kidney. We have conducted a retro and prospective study in order to identify the possible risk factors that can cause renal function impairment in young patients (18-40 years) with unilateral ureteral lithiasis obstruction and a normal contralateral kidney. Results. From 402 patients included in the study, 20.64% (83 cases) presented with serum creatinine ] 1.3 mg/dL. In patients with renal impairment, prevalence of male gender and history of NSAIDS use before admission were significantly higher than in non-AKI group. Serum urea/creatinine ratio, and estimated glomerular filtration rate (MDRD formula) were significantly higher, and respectively lower in AKI group. We found no significant differences between the two groups regarding age, prevalence of urinary tract infection after relief of obstruction, C-reactive protein value, and the duration of hospitalization. Conclusions. AKI in young patients with unilateral ureteral lithiasis obstruction and normal contralateral kidney is not quite a rare finding in our region. NSAIDs use can influence development of AKI, and should be used cautiously even in young patients with renal colic. In our opinion, the presence of AKI in patients with unilateral hydronephrosis demands urgent endourological intervention. Choosing conservative therapy in these patients, especially treatment with NSAIDS may aggravate the renal dysfunction.


2019 ◽  
Vol 48 (4) ◽  
pp. 030006051988810 ◽  
Author(s):  
Shang-Feng Tsai ◽  
Jun-Li Tsai ◽  
Cheng-Hsu Chen

Rhabdomyolysis is diagnosed based on the levels of blood biomarkers such as creatine kinase (CK), but the use of CK levels to predict long-term renal function remains controversial. This current report presents a case with a very high CK level with the presentation of acute kidney injury (AKI) who regained full renal function. A 29-year-old man, in a manic mood and presenting with dyspnoea, was admitted to hospital following an episode of ketamine use along with a history of drug abuse. The laboratory analyses identified rhabdomyolysis (CK, 35 266 U/l) and AKI (serum creatinine, 3.96 mg/dl). Despite treatment with intravenous normal saline (4000 ml/day), his CK level reached at least 300 000 U/l. He underwent 13 sessions of haemodialysis and his renal function fully recovered. The final measurements were serum creatinine 1.0 mg/dl and CK 212 U/l. These findings support the view that the predictive power of CK level on AKI is limited, especially regarding long-term renal function. Close follow-up examinations of renal function after haemodialysis are mandatory for patients with rhabdomyolysis.


2020 ◽  
Vol 318 (4) ◽  
pp. F1017-F1029 ◽  
Author(s):  
Judit Hodrea ◽  
Dora B. Balogh ◽  
Adam Hosszu ◽  
Lilla Lenart ◽  
Balazs Besztercei ◽  
...  

Diabetic kidney disease is a worldwide epidemic, and therapies are incomplete. Clinical data suggest that improved renal outcomes by Na+-glucose cotransporter 2 inhibitor (SGLT2i) are partly beyond their antihyperglycemic effects; however, the mechanisms are still elusive. Here, we investigated the effect of the SGLT2i dapagliflozin (DAPA) in the prevention of elevated O-GlcNAcylation and tubular hypoxia as contributors of renal fibrosis. Type 1 diabetes was induced by streptozotocin in adult male Wistar rats. After the onset of diabetes, rats were treated for 6 wk with DAPA or DAPA combined with losartan (LOS). The effect of hyperglycemia was tested in HK-2 cells kept under normal or high glucose conditions. To test the effect of hypoxia, cells were kept in 1% O2 for 2 h. Cells were treated with DAPA or DAPA combined with LOS. DAPA slowed the loss of renal function, mitigated renal tubular injury markers (kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin), and reduced tubulointerstitial fibrosis. DAPA diminished high glucose-induced protein O-GlcNAcylation and moderated the tubular response to hypoxia through the hypoxia-inducible factor pathway. DAPA alone was as effective as combined treatment with LOS in all outcome parameters. These data highlight the role of ameliorated O-GlcNAcylation and diminished tubular hypoxia as important benefits of SGLT2i treatment. Our results support the link between glucose toxicity, tubular hypoxia, and fibrosis, a vicious trio that could be targeted by SGLT2i in kidney diseases of other origins as well.


2020 ◽  
Vol 15 (9) ◽  
pp. 1240-1250 ◽  
Author(s):  
Caroline Liu ◽  
Maria K. Mor ◽  
Paul M. Palevsky ◽  
James S. Kaufman ◽  
Heather Thiessen Philbrook ◽  
...  

Background and objectivesIt is unknown whether iodinated contrast causes kidney parenchymal damage. Biomarkers that are more specific to nephron injury than serum creatinine may provide insight into whether contrast-associated AKI reflects tubular damage. We assessed the association between biomarker changes after contrast angiography with contrast-associated AKI and 90-day major adverse kidney events and death.Design, setting, participants, & measurementsWe conducted a longitudinal analysis of participants from the biomarker substudy of the Prevention of Serious Adverse Events following Angiography trial. We measured injury (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, IL-18) and repair (monocyte chemoattractant protein-1, uromodulin, YKL-40) proteins from plasma and urine samples at baseline and 2–4 hours postangiography. We assessed the associations between absolute changes and relative ratios of biomarkers with contrast-associated AKI and 90-day major adverse kidney events and death.ResultsParticipants (n=922) were predominately men (97%) with diabetes (82%). Mean age was 70±8 years, and eGFR was 48±13 ml/min per 1.73 m2; 73 (8%) and 60 (7%) participants experienced contrast-associated AKI and 90-day major adverse kidney events and death, respectively. No postangiography urine biomarkers were associated with contrast-associated AKI. Postangiography plasma kidney injury molecule-1 and IL-18 were significantly higher in participants with contrast-associated AKI compared with those who did not develop contrast-associated AKI: 428 (248, 745) versus 306 (179, 567) mg/dl; P=0.04 and 325 (247, 422) versus 280 (212, 366) mg/dl; P=0.009, respectively. The majority of patients did not experience an increase in urine or plasma biomarkers. Absolute changes in plasma IL-18 were comparable in participants with contrast-associated AKI (−30 [−71, −9] mg/dl) and those without contrast-associated AKI (−27 [−53, −10] mg/dl; P=0.62). Relative ratios of plasma IL-18 were also comparable in participants with contrast-associated AKI (0.91; 0.86, 0.97) and those without contrast-associated AKI (0.91; 0.85, 0.96; P=0.54).ConclusionsThe lack of significant differences in the absolute changes and relative ratios of injury and repair biomarkers by contrast-associated AKI status suggests that the majority of mild contrast-associated AKI cases may be driven by hemodynamic changes at the kidney.


2013 ◽  
Vol 35 ◽  
pp. 567-572 ◽  
Author(s):  
Sanja Simic Ogrizovic ◽  
Suzana Bojic ◽  
Gordana Basta-Jovanovic ◽  
Sanja Radojevic ◽  
Jelena Pavlovic ◽  
...  

Objectives. Retrospective study was designed to examine the importance of tissue kidney injury molecule-1 (KIM-1) expression in predicting kidney function in sixty patients (27 males) aged 34.15 ± 12.23 years with different kidney diseases over three years after kidney biopsy.Materials and Methods. Tissue KIM-1 expression was determined immunohistochemically and KIM-1 staining was scored semiquantitatively, as well as tubulointerstitialis (TIN), inflammation, atrophy, and fibrosis. Kidney function (MDRD formula) and proteinuria/day were evaluated at the time of biopsy (GFR0) and 6, 12, 24, and 36 months later.Results. Significantly positive correlations between tissue KIM-1 expression and age (r=0.313), TIN inflammation (r=0.456), fibrosis (r=0.317), and proteinuria at 6 months (r=0.394) as well as negative correlations with GFR0 (r=−0.572), GFR6 (r=−0.442), GFR24 (r=−0.398), and GFR36 (r=−0.412) were found. Meanwhile, TIN inflammation was the best predictor of all measured kidney functions during three years, while tissue KIM-1 expression (P=0.016) was a predictor only at 6 months after biopsy.Conclusion. Tissue KIM-1 expression significantly predicts kidney function solely at 6 months after biopsy, when the effects of immune and nonimmune treatments are the strongest.


2020 ◽  
Vol 10 (4) ◽  
pp. 221-224
Author(s):  
Kamel El-Reshaid ◽  
Shaikha Al-Bader

Acute kidney injury (AKI) indicates its abrupt deterioration and is defined as an increase in serum creatinine more than the baseline by > 26 umol/L within 48 hours or > 50% within 1 week.  The latter since glomerular failure is the life-threatening one with: (a) uremic intoxication, (b) water and salt retention with fluid overload, and (c) potassium accumulation with cardiac arrest.  The etiology can be pre-renal, post-renal or intrinsic.  Diagnosis is established by history of new insults, physical examination for hydration status, systemic stability and manifestations of autoimmune diseases/infections as well as an initial laboratory testing for renal function (serum creatinine, electrolytes and urine routine) and kidney ultrasound.  Additional specific tests are indicated to assess etiology of AKI and its associated co-morbid conditions that interacts with its management.  Severity of AKI ranges from mild (stage 1) to advanced (stage 5) that requires dialytic support.  Moreover, it depends on the type and duration of the insult.  Prognosis depends on etiology of AKI, its co-morbid conditions and the timely interventions by the supportive medical team.  Keywords: acute, causes, epidemiology, injury, kidney, management.


2021 ◽  
Vol 11 ◽  
Author(s):  
Rachel V. Jimenez ◽  
Alexander J. Szalai

In the blood of healthy individuals C-reactive protein (CRP) is typically quite scarce, whereas its blood concentration can rise robustly and rapidly in response to tissue damage and inflammation associated with trauma and infectious and non-infectious diseases. Consequently, CRP plasma or serum levels are routinely monitored in inpatients to gauge the severity of their initial illness and injury and their subsequent response to therapy and return to health. Its clinical utility as a faithful barometer of inflammation notwithstanding, it is often wrongly concluded that the biological actions of CRP (whatever they may be) are manifested only when blood CRP is elevated. In fact over the last decades, studies done in humans and animals (e.g. human CRP transgenic and CRP knockout mice) have shown that CRP is an important mediator of biological activities even in the absence of significant blood elevation, i.e. even at baseline levels. In this review we briefly recap the history of CRP, including a description of its discovery, early clinical use, and biosynthesis at baseline and during the acute phase response. Next we overview evidence that we and others have generated using animal models of arthritis, neointimal hyperplasia, and acute kidney injury that baseline CRP exerts important biological effects. In closing we discuss the possibility that therapeutic lowering of baseline CRP might be a useful way to treat certain diseases, including cancer.


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